Oxidative stress or KEAP1 inactivation (by its loss-of-function mutation, deletion, or epigenetic silencing in cancers) stabilizes NRF2, which subsequently translocates into the nucleus and promotes the transcription of a host of genes governing antioxidant defense and redox maintenance26–28, including genes involved in ferroptosis suppression29. The gene discussed is NFE2L2; the disease is cancer.